4.8 Article

Opa1-mediated cristae opening is Bax/Bak and BH3 dependent, required for apoptosis, and independent of Bak oligomerization

Journal

MOLECULAR CELL
Volume 31, Issue 4, Pages 557-569

Publisher

CELL PRESS
DOI: 10.1016/j.molcel.2008.07.010

Keywords

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Funding

  1. NIH [GM50284, GM62289, RR04050, DK54441]
  2. Leukemia and Lymphoma Society [7028-05]
  3. National Institute of Environmental Health Sciences (NIEHS) [ES010337]

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Controversy surrounds the role and mechanism of mitochondrial cristae remodeling in apoptosis. Here we show that the proapoptotic BH3-only proteins Bid and Bim induced full cytochrome c release but only a subtle alteration of crista junctions, which involved the disassembly of Opa1 complexes. Both mitochondrial outer membrane permeabilization (MOMP) and crista junction opening (CJO) were caspase independent and required a functional BH3 domain and Bax/Bak. However, MOMP and CJO were experimentally separable. Pharmacological blockade of MOMP did not prevent Opa1 disassembly and CJO; moreover, expression of a disassembly-resistant mutant Opa1 (Q297V) blocked cytochrome c release and apoptosis but not Bax activation. Thus, apoptosis requires a subtle form of Opa1-dependent crista remodeling that is induced by BH3-only proteins and Bax/Bak but independent of MOMP.

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